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Colorectal Cancer Screening (PDQ®)

Significance

Colorectal cancer (CRC) is the third most common malignant neoplasm worldwide [1] and
the second leading cause of cancer deaths in the United States.[2] It is
estimated that there will be 132,700 new cases diagnosed in the United States in 2015 and 49,700 deaths due to this disease. From 2007 to 2011, CRC incidence declined by 4.3% per year among adults aged 50 years and
older. However, in adults younger than 50 years, CRC incidence rates have been increasing by 1.8% per year. From 2007 to 2011, mortality from CRC
declined by 2.5% per year.[2] The
incidence is higher in men than in women. It ranges from 45.9 per 100,000 per
year in Hispanic men to 62.3 per 100,000 per year in African American men. In women, it ranges from
31.4 per 100,000 per year in Hispanics to 47.5 per 100,000 per year in African Americans.
The
age-adjusted mortality rates is 19.1 per 100,000 per year in men and 13.5 per 100,000 per year in
women.[3] About 5% of Americans are expected to develop the disease within
their lifetime and about half of those will die from it.[3] Age-specific incidence and mortality rates show that the vast majority of
cases are diagnosed after age 50 years; about 4% of CRCs occur younger than age 50 years.[4,5]

Among the groups that have a high incidence of CRC are those with hereditary conditions, such as familial adenomatous
polyposis and hereditary nonpolyposis CRC (inherited in an
autosomal dominant manner). Combined, the two groups account for no more than 6% of
CRCs. More common conditions associated with an increased risk
include a personal history of CRC or adenomas; first-degree
relative with CRC; a personal history of ovarian, endometrial, or
breast cancer; and a personal history of long-standing chronic ulcerative
colitis or Crohn colitis.[6-8] These high-risk groups account for about a
quarter of all CRCs. Limiting screening or early cancer
detection to only these high-risk groups would miss the majority of CRCs.[9]

Genetic,[10] experimental, and epidemiologic [11] studies suggest that
CRC results from complex interactions between inherited
susceptibility and environmental or lifestyle factors. Efforts to identify
causes led to the hypothesis
that adenomatous polyps (adenomas) are precursors for the vast majority of
CRCs.[12] In effect, measures that reduce the incidence and
prevalence of adenomas may result in a subsequent decrease in the risk of
CRCs;[13] however, some CRC mortality may be caused by fast-growing lesions and even lesions that do not pass through an adenomatous phase. Overall, the details of growth rates of adenomas and cancer are unknown; most likely there is a broad spectrum of growth patterns, including formation and spontaneous regression of adenomas.[14]